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Old Mar 23, 2006 | 09:47 PM
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Default FS: 1999 Civic EX, 5spd, Stock, 120k, loaded>>5K/OBO

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Old Mar 25, 2006 | 03:17 PM
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Old Mar 28, 2006 | 01:59 PM
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Default Re: FS: 1999 Civic EX, 5spd, Stock, 120k, loaded>>5K/OBO (SkyLinER)

Pictures UP
Old Mar 28, 2006 | 05:01 PM
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Default Re: FS: 1999 Civic EX, 5spd, Stock, 120k, loaded>>5K/OBO (SkyLinER)

bump before dinner...
Old Mar 28, 2006 | 06:11 PM
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all pm replied
Old Apr 3, 2006 | 03:08 PM
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Old Apr 6, 2006 | 09:41 PM
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Default Re: FS: 1999 Civic EX, 5spd, Stock, 120k, loaded>>5K/OBO (SkyLinER)

bump bump bump
Old Apr 7, 2006 | 06:22 AM
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Default Re: FS: 1999 Civic EX, 5spd, Stock, 120k, loaded>>5K/OBO (SkyLinER)

TRADE??


http://hondamarketplace.com/zerothread?id=1567538
Old Apr 8, 2006 | 07:02 PM
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Default Re: FS: 1999 Civic EX, 5spd, Stock, 120k, loaded>>5K/OBO (SkyLinER)

bump
Old Apr 11, 2006 | 09:49 PM
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Default Re: FS: 1999 Civic EX, 5spd, Stock, 120k, loaded>>5K/OBO (SkyLinER)

www
Old Apr 13, 2006 | 06:54 AM
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Default Re: FS: 1999 Civic EX, 5spd, Stock, 120k, loaded>>5K/OBO (SkyLinER)

bumo
Old Apr 15, 2006 | 12:11 PM
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Default Re: FS: 1999 Civic EX, 5spd, Stock, 120k, loaded>>5K/OBO (SkyLinER)

wa le ca le ho li ba ma cac ban him she to lai
Old Apr 21, 2006 | 06:12 PM
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Old Apr 27, 2006 | 07:44 PM
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Old May 1, 2006 | 06:07 PM
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Default Re: FS: 1999 Civic EX, 5spd, Stock, 120k, loaded>>5K/OBO (SkyLinER)

yup
Old May 1, 2006 | 06:46 PM
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Default Re: FS: 1999 Civic EX, 5spd, Stock, 120k, loaded>>5K/OBO (SkyLinER)


Gynecological
[1] Structure and function of the female reproductive system
OvariesàFallopian tubeàuterusàvagina
Ovaries(2): production of eggs and ovulation. Ovaries alternate in producing eggs. It also produces estrogen and progestin. Each ovary has a fallopian tube.
Fallopian Tube(2): this is where egg get fertilized
Uterus(1): fertilized egg comes to term
Corpus-upper, longer part of uterus, secretes progesterone
Cervix-lower part of the uterus
Endometrium- lining of the uterus
Myometrium-smooth muscle
Perimetrium- outer lining of uterus
Vagina: birth canal that is continuous w/ external environment
[2] Menstrual Disorders:
*menstrual cycle begins @ menarche and continues into menopause. It includes the maturation and release of oocytes from the ovary during ovulation and periodic vaginal bleeding resulting from shedding of the endometrial lining. Minimum body weight (48kg) and fat content (16%-24%) are necessary for menarche to occur and for menstrual cycle to maintain.
*The menstrual cycle is controlled by rhythmic synthesis and release of ovarian hormones (estrogen and progesterone) under feedback control from the hypothalamic gonadotropin releasing hormone and the anterior pituitary gonadotropic follicle stimulating and lutinizing hormones.
A] Menstruation: monthly endometrial changes in anticipation of pregnancy. If no pregnancy occurs, altered endometrium is expelled along w/ 50-100 ml of blood.
Amennorrhea: absence of menstruation, this can be pathologic but is physiologic especially during pregnancy, prior to menarche (1st menstrual cycle b/t ages 11-14), post-menopausal (last menstrual cycle), w/ low % body fat (when body fat is too low, it disrupt hormones that are needed for pregnancy)
Natural menopause: permanent cessation of menstrual cycle.12 months later, 12 consecutive months w/ amenorrhea w/o pathologic etiology. Ovulation often ceases first. Hormonal declines (estrogen, progestin), not linear.
Perimenopause: onset is around the time of menopause. +/- 1 year from point of menopause. Characterizes by irregular menstrual changes.
Symptoms:
Hot Flushes/Flashes: sudden sensation of heat, sweating, flushing of face, neck, upper trunk. Episodes last 1-5 minutes and occur from 1-5 years. Can be objectively measured like * skin temp, moisture, change in color…all due to vascular instability-vasodilation.
Night Sweats: hot flashes that occur at night. Sweating is b/c moisture can’t escape, moisture weaks her up not heat.
Vaginal Changes: ¯ estrogen leads to atrophy and changes in normal vaginal secretions (¯ volume). Vagina is more sensitive, more tender.
Sexual interest (libido): ¯ interest due to vaginal sensitivity and * interest is due to no fear in pregnancy.
Urinary incontinence: internal sphincter is estrogen sensitive. Atrophy causes women to have loss of urinary control.
Mood changes: irritability, fatigue, severity has to do with hot flashes and night sweats. Begin at the time of menopause.
Signs:
Maturation index: histologic exam looking at cells of vaginal epithelium microscopically.
Vaginal pH: 6-7.5 w/o infectionàperimenopausal
Increase in FSH: if elevatedàperimenopausal
Estradiol changes: multiple readings are irregular, not consistent
Onset history: early menarche means later menopause. Familial. Long-term cigarette use may lead to earlier onset, smoking increase biotransformation of estrogens. Estrogenà androgen.
*hysterectomy-remove uterus, accelerate menopause, makes other symptoms occur earlier.
B] Premenstrual Tension Syndrome (PMS): fatigue, anger, irritability associated w/ menstruation- premenstrual
Premenstrual dysphoric disorder (PMDD): weight gain 6-8 lbs, swollen or tender breasts, headaches, abnormal abdominal swelling
C] Dysmenorrhea: menstrual cramps prior to or during mensis. Etiology is due to prostaglandin production that induces uterine contractions, this will act on myometrium to expel endometrium and activate nociceptors (pain receptors) that result in cramping. NSAIDs block prostaglandin production and prolong bleeding phase of the cycle b/c diminishing the extent of contraction
D] Toxic Shock Syndrome: it’s a form of septic shock caused by Staph. Bacteria. The higher absorptive tampons the greater the risk of infection. Absorption of vaginal secretions (as well as blood) which are antibacterial (natural defense is eliminated)
[3] Endometriosis: Ectopic endometrium. Found in fallopian tube, ovaries, and abdominal cavity. Retrograde menstruation, ectopic fragments are not destroyed. This triggers inflammation that causes pelvic pain that become disabling during mensis. Painful intercourse, urination, or defecation. Tx surgically remove displaced endometrium. High incidence of infertility.
[4] Vaginitis: itchy, tenderness, pain, abnormal discharge. This cause by bacteria, chemicals from swimming pools or over enthusiastic intercourse.
Candidiasis: “yeast” infection or white fungus. Leukorrhea (white discharge, Tx with antifungal). Not sexually transmitted. Etiology is by antibiotic use (vaginal microflora) give rise to suprainfection, immunocompromised state, poorly controlled diabetes (glucose spills in vagina secretion/ uterus causing an overgrowth)
Trichomoniasis: protozoan infection. Can be sexually transmitted. Males are asymptomatic. Flourishes in hot, warm environment like dry swimming suits. Flagella is easily recognized. Discharge grey-yellow, frothy, foul aroma
[5] Sexually Transmitted Disease (STDs)
commonly transmitted by sexual contact. If superficial lesions, it will develop 1st in mucous membranes at inoculation site. More than 10 million new STD cases reported annually from the center of disease control.
Incubation phase: no lesions, no transmission * no lesions doesn’t mean no trans.
Subclinial phase: no symptoms, but there is transmission
Dormant phase: with or without transmission
Gonorrhea: common bacterial from unprotected sex w/ multiple partners. Systemic complications includes fever, skin lesions, arthritis. Tx with antibiotic.
Symptom in men: urethral pain, burning w/ urination, profuse blood tinged urethral discharge, pronounced enough to seek medical attention.
Symptom in Women: milder symptoms, cranberry juice will relieve symptoms. dysuria, frequency, urgency. Discharge (not all women) is milder.
Nongonococcal urethritis (NGU) Chlamydia: etiology is bacterial like microorganism that responds to antibiotics. Intracellular growth. 700k cases/year reported. 150k newborns are afflicted w/ Chlamydia-eyes, ears, respiration. Symptoms is milder than gonorrhea. ¾ of women are asymptomatic. Incubation period is longer than gonorrhea (longer than 3 weeks). Tx with antibiotics.
Pelvic Inflammatory Disease (PID): complication of gonorrhea/chlamydia. Exclusively occurs in women, not in men. Salpingitis is inflammation of fallopian tube. Fallopian tube is open at the end, endometrium/microorangisms can move into area. Abdominal cramping, chills, fever, strong possible of infertility-6% for 1st episode up to 60% 3rd episode. Leading cause of infertility.
Syphilis: Sporochetes that occurs less than gonorrhea. Responsive to antibiotics and highly treatable
3 phases:
primary: chancere- superficial, painless but large lesions in area of inoculation site
secondary: can still use antibiotic
Tertiary: CNS involved, develop dementia
Condylomata: Genital Warts caused by human papilloma virus. 20 million cases in US, 30 serotypes. Treatment by excision of warts (surgically, freezing, laser). Dormant HPV and some serotypes are the etiology for 50% cervical cancer like HPV 16 and some colorectal cases also.
Herpes Genitalis: Herpes simplex virus #2 (HSV-2). It can become dormant and reactivated by immunosupression or stress (emotional or localized trauma). Lesions are multiple shallow ulcerations and become vesicles, itchy, painful. Tx with antivirals to decrease severity and accelerate healings.
Acquired immunodeficiency syndrome (AIDS):
-1/3 million of Americans and 40k new cases per year. Transmission most commonly between homosexual males and worldwide heterosexual transmission. Also with mother to child and other bodily secretions.
-Incubation: HIV enters CD4T cells and targeted during other STD outbreaks. People w/ other STD are more likely to contract HIV. HIV+ untreated can take as long as 7-9 yrs to have a full-blown case of AIDs.
-Effects of immunosupression leading to opportunistic diseases that are viruses, virally induced cancers, and other pathogens. Kaposis sarcoma, TB, candidiasis, aspergillosis
-treatments involves antiviral drugs in combination and prolong development of AIDs


[6] Uterine Cancer
Cervical Cancer: caused by HPV. Abnormal exfoliated cells in cervical smear (PAP smear) and can be detect pre-cancer and can diagnose prior to cancer so no infiltration, no metastasis. Leads to irregular bleeding…perimenopausal.
Endometrial Cancer: cancer of the uterine lining. More insidious and lifetime estrogen exposure is correlated to incidence. Early menarche. Non parous means no kids, higher exposure to estrogen. Excess adipose (estrogen stored in adipose). 1st degree relatives w/ endometrial cancer. It has same risk factors as breast cancer.
[7] Cystic Hyperplasia: fibrocystic breast disease, tend to occur as multiple lumps and tend to vary cyclically, it is painful during menstruation due to fluid filled. Aspirating (stick needle in to find fluid), can’t tell by touching.
[8] Carcinoma of the breast: 12% lifetime incidence and 2/3 of the cases within 5 yrs of menopause. Detectable lump began as a single cancer cell 8-10 yrs earlier.
-Known genes:
BRCA I (ER -)-estrogen has nothing to do with this.
BRCA II (ER+)- account for only 10% of cases and stimulated by estrogen
*ER=estrogen receptor
-Tumor occurs in the upper outer quadriant and can be ductal (milk delivery, infiltrating-in situ w/in a duct) or lobular (site of milk production).
-prognosis depends on size and lymph node involvement, early recovery means higher cure rate. Chemotherapy, males< 0.1% rate of women.

Endocrine

[1] Introduction:
secretory: hormones, cytokine, and neurotransmitters
all secretions have tissues that are targets (availability of receptors). Hormones circulate in bloodstream can get to tissues. Tissue most influenced are tissues w/ highest number of receptors. The tissue with the most receptors means most pronounced changes. There are 2 types of receptors: 1) cell surface receptor- rapid response
2) cytosolic receptors- delayed response (24hrs) inside the cell, hormone receptor that influences DNA and altering expressions of some gene, thus protein production is altered.
Hormones produced all the time but rapid/delayed deals w/ how quickly we see response. Use both types of receptors- estrogen (vascular response on cell surface and trophic response by cytosolic receptors)
[2] Disorders of the endocrine system
Hormone deficiency states (hypofunction)
1. Hypofunction of endocrine glands: under production of the hormone
2. Extraglandular disorders: prohormones are inadequately converted to hormones causing defiency. Accelerated inactivation-metabolized too rapidly.
3. Hyporesponsiveness to hormones: problems w/ receptor #, receptor affinity, and cell signaling.
Hormone excess syndromes (hyperfunction)
1. Hyperfunction of endocrine glands: hyperplasia of secreting cells, adenoma (glandular tumor) tend to hypersecrete
2. Ectopic hormone production: secreting cells emerge outside of the endocrine gland proper- too much hormone being processed.
Assessment: history, symptomology, 2nd look at hormone levels and responsivness, tachycardia. Where is the problem coming from is the 1st decision- hard to assess.
Therapy: replacement if there is a deficiency. Glandectomy or antagonists if there’s an exess.
[3] Neurohypophysis (posterior pituitary)
Antidiruetic hormone (ADH, Vasopressin)
Synthesized by the hypothalamus and transported to posterior pituitary (where it is stored and subsequent to release. 2 principle targets: blood vessels, vasopressin cause vessels to constrict, acting on V1 receptor (good vasoconstrictor, but not needed) and V2 receptor (collecting duct ADH, aquaphorin molecules are expressed for water transport. Reabsorpion on collecting duct. No ADH 1.8L urineà 18 L urine
Diabetes Insipidus (tasteless urine)
Deficiency of ADH, conflicts young males. Excess thirst in which craving for ice water, large volumes of urine w/ low specific gravity. “sipide” means tasteless. Polyuria (excessive urination) and polydipsia (excessive thirst). Hypothalamic malfunction in which hypothalamus not producing enough ADH. Adverse reaction to lithium. Treatment is go with the craving, replace ADH. People can live with it, just need to suck it up.
[4] Adrenal Cortex (outer portion of adrenal gland)
Adrenals and endocrine function:
Corticosteroids-promiscuity-interact/occupy other receptors.
Salt: mineralocorticoids, aldosterone increase Na+ and H2O retention, K+ loss. Tendency to produce edema, retain fluid b/c too much salt. 2o cause of hypertension due to increase amount of aldosterone.
Stress/Sugar: influenced by glucocorticoids. Naturally, cortisol/hydrocortisone promotes glucose metabolism by glugoneogenesis. Ability to withstand from stress such as trauma, inflammation, and shock by produced corisol
Sex: androgen is a masculanizing hormone produced by both men and women. hypersecretion in females is called virilism- masculanization in femal and male children





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